Abstract

Circulating catecholamine that is increased in early phase of myocardial infarction alters serum electrolyte levels which might predispose to serious ventricular arrhythmias. In this study the effect of pretreatment of carvedilol on adrenaline-induced changes in the serum electrolytes (Mg2+, K+, Ca2+, Na+) was evaluated in rats. Adrenaline was administered at a dose of 2 mg/kg body weight subcutaneously 2 injections 24 hours apart and serum electrolytes were estimated at 12 hours, 24 hours and 7 days after the 2nd injection of adrenaline. Adrenaline administration initially caused hypomagnesemia, hypokalemia, hypocalcemia and hyponatremia, which were restored to normal spontaneously within 7 days. Pretreatment of carvedilol orally at a dose of 1 mg/kg body weight for 2 weeks significantly prevented initial reduction in serum electrolyte levels induced by adrenaline. It was concluded that prophylactic use of carvedilol might prevent the serious consequences of myocardial infarction as sudden cardiac death due to arrhythmia caused by electrolyte changes.

Highlights

  • IntroductionSudden cardiac death is the most common fatal outcome of ischemic heart disease

  • Ischemic heart disease is an emerging health problem in Bangladesh[1]

  • Patients with higher plasma catecholamine level within the 1st few hours of acute myocardial infarction subsequently appear to have greater myocardial damage and higher mortality rate. This evidence supports the concept that catecholamine may exert a deleterious effect[4] and higher catecholamine level leads to myocardial ischemia, which may contribute to the genesis of ventricular fibrillation[5]

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Summary

Introduction

Sudden cardiac death is the most common fatal outcome of ischemic heart disease. Ventricular fibrillation is a potentially fatal cardiac arrhythmia during the acute stage of myocardial infarction and is the most common cause of sudden death resulting from sudden cardiac syncope[3]. Patients with higher plasma catecholamine level within the 1st few hours of acute myocardial infarction subsequently appear to have greater myocardial damage and higher mortality rate. This evidence supports the concept that catecholamine may exert a deleterious effect[4] and higher catecholamine level leads to myocardial ischemia, which may contribute to the genesis of ventricular fibrillation[5]

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